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H Sohmer

Publications and source records attributed to H Sohmer.

At least 37 records · Page 2Linked to original sources
PubMed1999

Surgical anatomy of the ear of the fat sand rat.

OBJECTIVE: This study was conducted to investigate and describe the anatomical details of the ear of the fat sand rat (Psammomys obesus). METHODS: Thirty ears (15 in dry skull and 15 in live animals) were dissected with the aid of an operating microscope and microsurgical techniques. Photographs were taken through an operating microscope. RESULTS: The temporal bone of the fat sand rat consists mainly of an unusually large bulla. Three distinct auditory ossicles were visualized and the manubrium of the malleus is relatively long in relation to the size of the ear. Most parts of the inner ear bulge into the bulla cavity and are easily accessible. The cochlea consists of 3.25 turns. The tympanic membrane, facial nerve, stapedial artery, and eustachian tube are described in detail. The large size of the bulla is probably related to the high sensitivity, particularly at low frequencies of the animals ear. CONCLUSION: The fat sand rat was found to be an excellent experimental animal for the investigation of middle and inner ear physiology.

Animals↗
PubMed1999

The effect of head orientation on the vestibular evoked potentials to linear acceleration impulses in rats.

OBJECTIVE: To investigate the influence of linear acceleration impulses delivered when the head is held in different static head orientations, on the first wave of the short latency vestibular evoked potential (VsEP). The first wave is the compound action potential of the primary vestibular neurons synchronously activated. BACKGROUND: It has been shown previously that the VsEP elicited in response to linear acceleration is initiated mainly in the otolith organs. These organs are responsive to both dynamic and static linear forces, including gravity. METHODS: VsEPs to linear acceleration stimuli (4g) were recorded when the rats head was oriented so that a) the plane of the utricular macula was aligned with the plane of the stimulus, b) in supine position and c) with the head pitched up and down in various angles with respect to gravity (stimulus-head spatial relation remained constant) as compared to a reference position. RESULTS: With the stimulus aligned with the plane of the utricular macula, the amplitude of the first wave of the L-VsEPs was significantly larger than in the reference position. In the supine position, the amplitude of the first wave was significantly larger and the latency was significantly shorter. The amplitude of the first VsEP wave tended to be larger in the "head up" orientations as compared to the "head down" orientations (not statistically significant). CONCLUSIONS: These results demonstrate the influence of head position and gravity on the VsEPs to linear acceleration impulses, which is in accordance with their otolithic origin.

Acceleration↗
PubMed1999

Differential effect of the loop diuretic furosemide on short latency auditory and vestibular-evoked potentials.

OBJECTIVE: This study aimed to investigate the differential effect of the loop diuretic furosemide on the auditory and vestibular (otolith) end organs in the same animals simultaneously. DESIGN AND METHODS: Auditory nerve-brain stem-evoked responses (ABR-generated in the cochlea) and short latency vestibular-evoked responses to linear acceleration impulses (L-VsEP-generated in the otolith organs) were recorded from albino Sabra rats both before and at minute intervals after intravenous injections of the loop diuretic furosemide. In some animals, an equal volume of saline was injected to control for the effect of the injection itself. In most animals, more than one injection of saline or furosemide was possible (furosemide, N = 17 injections in 10 rats; saline, N = 18 injections in 9 rats). Peak-to-peak amplitude and peak latency changes in the first wave in each recording (representing end-organ activity) as a function of postinjection time were compared between the two evoked potentials using analysis of variance and repeated t-tests. RESULTS: Saline injections caused only minor changes in the amplitude of the ABR and the L-VsEP. After administration of furosemide, the amplitude of the L-VsEP hardly changed. However, there was a noticeable decrease in the amplitude of the ABR. CONCLUSIONS: Although furosemide has a major depressant effect on cochlear function, vestibular end-organ activity is hardly altered.

Analysis of Variance↗
PubMed1997

Short latency vestibular evoked potentials (VsEPs) to linear acceleration impulses in rats.

In this study, short latency (t < 12.7 ms) vestibular evoked potentials (VsEPs) in response to linear acceleration impulses were recorded in 37 rats. A new technique (based on a solenoid) was used for generating linear force impulses that were delivered to the animal's head. The impulse had a maximal peak acceleration of 12 g. During the impulse, the displacement was 50 microns (at 4 g) and the rise time was 1.0 ms. A stimulation rate of 2/s was usually used. The VsEPs (averaged responses to 128 stimulations, digital filter: 300-1500 Hz) were recorded with electrodes on pinna and vertex, and were composed of 4-6 clear waves with mean amplitudes (for a 4 g stimulus) of 1-5 microV. The VsEPs were resistant to white noise masking, and were significantly suppressed (P < 0.05) following bilateral application of a saturated KCl solution to the inner ear, showing that contributions of the auditory and somatosensory systems are negligible. The latency of the response decreased as a power law function of stimulus magnitude, and the amplitude of the first wave increased as a sigmoid function of stimulus magnitude. VsEP responses were still present at the lowest intensities attainable (0.06-0.4 g) and reached saturation at 9 g. The amplitude of the later components was reduced when stimulus rate was elevated to 20/s. These results suggest that VsEPs in response to linear accelerations are similar in their nature to VsEPs in response to angular acceleration impulses that were previously recorded. These VsEPs to linear accelerations are most likely initiated in the otolith organs.

Acceleration↗
PubMed1997

Contribution of the eighth nerve and cranial nerve nuclei to the short-latency vestibular evoked potentials in cats.

The object of this study was to assess the contributions of the vestibular nerve and various cranial nerve nuclei to the short-latency vestibular evoked potentials in cat. The following nuclei were investigated: vestibular nuclei and the third, sixth, and tenth cranial nerve nuclei. In unilateral labyrinthectomized cats, we performed suboccipital craniectomy and partial cerebellectomy to place bipolar electrodes into the neural structures under investigation. The surface-recorded vestibular evoked potentials (far field) were compared with the potentials recorded intracranially in response to the same acceleration impulses. The exact locations were later confirmed histologically. Reversible lesions also were induced by injection of lidocaine 2%. The results indicate that the first wave of the vestibular evoked potentials originates in the vestibular nerve, and the second wave is mainly generated in the superior and medial vestibular nuclei. The third, sixth, and tenth cranial nerve nuclei apparently contribute to the later waves of the vestibular evoked potentials, particularly waves 3 and 4.

Abducens Nerve↗
PubMed1997

Somatosensory functioning in children with attention deficit hyperactivity disorder.

In order to test the hypothesis that attention deficit hyperactivity disorder (ADHD) is related to deficits in somatosensory processing, 49 ADHD male children and 49 matched controls were tested on a wide range of tactile tasks, and somatosensory evoked potentials (SEP) were also recorded. In addition, parents' and teachers' ratings on the children's typical responses to tactile stimuli were obtained. The results show that the ADHD children were less skilled on suprathreshold, but not on threshold tasks than were the controls. Further, a larger percentage of ADHD children were 'tactile defensive'. Finally, the ADHD children showed larger-than-normal amplitudes of late, but not early components of the SEP. These data suggest that some aspects of somatosensory processing by ADHD children are deficient.

Attention Deficit Disorder with Hyperactivity↗
PubMed1997

Pathophysiological mechanisms of hearing loss.

An understanding of auditory transduction in the ear can contribute to a better comprehension of the pathophysiological mechanisms which give rise to hearing loss. The incoming sound sets up a mechanical traveling wave which begins at the base and progresses along the basilar membrane, reaching a point of maximal displacement. The region of maximal displacement is a function of stimulus frequency. The mechanical displacement, by directly opening ion channels in the stereocilia of the hair cells, induces changes in the electrical potential of the hair cells. This initial stage is called mechano-electrical transduction, and in the normal ear, is followed by a stage of electro-mechanical transduction based on the ability of the outer hair cells to respond to the electrical changes induced in them with a change in their length. This "electromotility" presumably provides mechanical feedback to the basilar membrane, augmenting its mechanical displacement. This is called the cochlear amplifier, providing the ear with improved sensitivity and frequency discrimination. Most forms of sensori-neural hearing losses (affecting the inner ear) are due to a lesion to some part of this cochlear amplifier (e.g. noise induced hearing loss, ototoxic drugs) and are therefore characterized by auditory threshold elevations and poorer frequency discrimination.

Acoustic Stimulation↗
PubMed1997

Cooling induces a decrease in middle ear compliance.

The effects of cooling rats from 37 degrees C to 27 degrees C and rewarming to 37 degrees C on the conductive mechanism of the middle ear was studied by means of acoustic impedance measurements. Cooling reduced middle ear compliance reversibly, without an effect on external canal volume and middle ear pressure. These results provide evidence for an increase in the stiffness of the tympanic membrane and/or of the ossicular chain and/or a decrease in stapes mobility. Thus a small part of the decrease in the magnitude of otoacoustic emissions during cooling is due to an effect on the conductive mechanism of the middle ear.

Acoustic Impedance Tests↗
PubMed1996

Vertical plane short and middle latency vestibular evoked potentials in humans.

In order to determine whether short and middle latency vestibular evoked potentials (VsEPs) can be recorded in humans in response to angular acceleration stimuli in the vertical plane, a drum, head-holder, and stepper motor were designed to deliver upward acceleration impulses of 10,000 degrees/s2 (1.8 degrees displacement) to the human head. Forehead and mastoid electrodes recorded electrical activity that was filtered, differentially amplified, and averaged in short (12.7 milliseconds) and middle (63.5 milliseconds) latency time frames. Control recordings were used to eliminate various types of artifact. Recordings were conducted in 7 normal subjects and in 4 control patients with congenital, profound hearing loss and absence of caloric responses. Short and middle latency VsEPs with high intrasubject and intersubject consistency were recorded in normal subjects and not in control patients. The middle latency responses were larger in amplitude than the short latency responses. The effects of stimulus intensity and repetition rate on VsEP waveform, latency, and amplitude studied. Experiments have shown that the responses are not electrical artifact, nor are they contaminated by auditory, somatosensory, or passive eye movement potentials.

Acceleration↗
PubMed1996

Postnatal development of somatosensory evoked potential in jaundiced Gunn rats and effects of sulfadimethoxine administration.

Bilirubin encephalopathy results from the entry of bilirubin into the brain and is expressed by motor, sensory, and/or behavioral impairment. The jaundiced (jj) Gunn rat is a valuable animal model for studying the kinetics of bilirubin-induced neurotoxicity. This is often done by recording evoked potentials, which are also used as indices of brain damage in infants who develop neonatal jaundice, as is the case with the auditory nerve and brainstem evoked response (ABR). The present study describes the postnatal development of the somatosensory evoked potential (SEP) in Gunn rats. No effects of jaundice on the SEP were found in young jj rats (16-28 d). However, adult (3-4 mo) jj rats had prolonged latencies and decreased amplitudes of the P2 component of the SEP compared with adult nonjaundiced (Jj) rats. These changes in the SEP of jaundiced rats may reflect a synaptic lesion in these animals, possibly due to cumulative and/or progressive damage induced by bilirubin during the first 3 mo of life. After sulfadimethoxine administration, marked latency prolongations (2-6%) were observed in the early components of SEP in young (3-wk-old) jj (but not Jj) rats, as early as 2 h after injection. These changes, which became more severe (4-10%) with time, seem to be mostly peripheral. The present results suggest that the SEP may be a sensitive marker for the massive entry of bilirubin into the nervous system, and could serve as part of an evoked potential battery (in addition to visual evoked potential and ABR) in assessing bilirubin-induced neurotoxicity in jaundiced newborns and infants.

Animals↗
PubMed1996

The role of adrenocortical steroid hormones in the development of hearing.

Based on the findings that adrenocortical hormones are involved in the regulation of Na+, K(+)-ATPase in several tissues and the presence of receptors for these hormones in the ear during auditory development, it has been suggested that these hormones also induce Na+, K(+)-ATPase activity and the endocochlear potential in the ear, leading to auditory function in the fetus-neonate. In order to test this hypothesis, glucocorticoid and mineralocorticoid hormones were injected into rat pups and their auditory development, compared to control litter-mates, was tested by recording auditory nerve-brainstem evoked potentials (ABR). Those who received glucocorticoid hormones had elevated ABR thresholds on post-natal day (PND) 9, others on PND 11 and still others on PND 16, compared to control litter-mates. The ABR thresholds of those injected with mineralocorticoids were not different from those in controls. These results and additional considerations related to the time sequence of the natural appearance of these hormones in the plasma, of their receptors in the ear and the onset of hearing in rat pups makes it extremely unlikely that adrenocortical hormones are involved in the initiation of Na+, K(+)-ATPase pumps and thereby of the endocochlear potential in the inner ear. It is possible that these hormones and their receptors play a role in the later regulation of the number of pumps.

Aldosterone↗
PubMed1996

Thyroxine affects physiological and morphological development of the ear.

The onset and development of distortion product otoacoustic emissions (DPE) representing cochlear amplifier activity were studied in neonatal hyperthyroid (n = 10) and control (n = 10) rat pups. These were compared to the onset and development of auditory nerve-brainstem evoked responses (ABR) representing overall cochlear function, and to morphological development of the ear. DPEs were recorded at an earlier postnatal age to high (8 kHz) frequencies and progressed to lower (3 kHz) frequencies with age. ABRs to high-intensity clicks were recorded at least 2 days before DPEs, although DPE onset at 8 kHz preceded adult-like ABR thresholds. Both ABR and DPEs appeared earlier in the hyperthyroid rats. Histological evidence showed earlier morphological development of the ear in these animals. ABR thresholds and DPE amplitudes matured at a slower rate in the experimental group despite their earlier onset. There was no difference in ABR and DPE thresholds between adult hyperthyroid and control rats. However, in the experimental group, DPEs had smaller amplitudes to high (70 dB SPL) and to low (50 dB SPL) stimulus intensities at low frequencies. Hence, despite thyroxine-injected rat pups having earlier onset of auditory structure and function (lower ABR thresholds and earlier functioning active cochlear amplifier), it appeared that neonatal hyperthyroidism affected the later state of the cochlea, such that DPEs, especially to low-frequency stimuli, were depressed during and after maturation.

Acoustic Stimulation↗
PubMed1996

Transient evoked otoacoustic emissions can be recorded in the rat.

Transient (click) evoked (TEOAE) and distortion product (DPOAE) otoacoustic emissions can be recorded in most normal human ears. Even though DPOAEs have been recorded in many laboratory animals, there has not been much success in recording TEOAEs in non-primate mammals except for guinea pigs. In this study, TEOAEs were unequivocally recorded in every rat (and guinea pig) ear studied by using short pulses (40 microseconds) to generate the clicks and a short (1.1 ms) amplifier gain suppression period. The responses were reproducible in the same rat, above the noise floor and disappeared post-mortem. They were shorter in duration in rats than in guinea pigs and were made up of a broadband frequency spectrum between 2 and 4 kHz. Post-mortem, the TEOAEs to 65 dB SPL clicks disappeared at about the same time as DPOAEs to low stimulus intensities and before the DPOAEs to high stimulus intensities. The ability to record TEOAEs in rats and other animals should permit further experimentation into the basic mechanisms of generation of otoacoustic emissions in general and TEOAEs in particular.

Acoustic Stimulation↗
PubMed1995

Peripheral generators of the vestibular evoked potentials in the cat.

OBJECTIVES: The contributions of each of the vertical semicircular canals (SCCs) and otoliths to the short-latency vestibular evoked potentials in response to angular acceleration impulses were studied in the cat. DESIGN: The experiments were conducted on unilateral labyrinthectomized cats. Vestibular activation was achieved by delivering angular acceleration impulses to the animal's head, held in the position presumed to be optimal for maximal stimulation of either the anterior or the posterior SCCs before and after obliteration of the SCC studied, and before and after obliteration of the other SCCs and ablation of the maculae. INTERVENTIONS: Unilateral labyrinthectomy, obliteration of the SCCs, and ablation of the otoliths and section of the commissural vestibular fibers in the brain stem with histologic confirmation were carried out in the experiments. RESULTS: Following selective obliteration of either the anterior or the posterior SCC of the remaining ear and stimulation in the presumed optimal plane of the obliterated canal, the early prominent waves (P1 and P2) disappeared, leaving only much smaller-amplitude waves. These were severely depressed after ablation of the maculae. On the other hand, the vestibular evoked potentials in response to excitatory stimuli were not affected by obliteration of the other two SCCs and ablation of the maculae. CONCLUSION: These results indicate that when the head is stimulated in the optimal plane of each of the SCCs, the vestibular evoked potentials are generated mainly by the cristae ampullaris being stimulated, while the otoliths contribute smaller responses.

Animals↗
PubMed1995

Effect of thyroxine on the development of somatosensory and visual evoked potentials in the rat.

The thyroid hormone thyroxine (T4), administered post-natally to neonatal rats, has been shown to accelerate development of auditory function, as expressed by auditory nerve-brainstem evoked responses. This study investigated whether this earlier development was also reflected in other sensory modalities. Rat pups were injected with T4 from the day of birth for 10 consecutive days. Somatosensory evoked potentials, both from the cortex and from sub-cortical structures, and flash-elicited visual evoked potentials (VEP), were recorded at various ages up to 3 months. The recordings were compared with those from control rats from the same litters. Only a minimal difference was found between the experimental and control groups, the most significant being in the VEP at age 12 days, by which time the eyes of most of the experimental rats had opened, which was not the case for the majority of control rats. This difference disappeared with eye-opening in the control rats. Although T4 is known to affect myelinization and synaptic transmission in developing rat brain, this apparently only minimally affects the functioning of the brain as expressed by evoked potentials, both in the short and long term. The main effect of neonatal hyperthyroidism in these rats appeared to be accelerated development of the end organ (the eye and the ear).

Age Factors↗
PubMed1995

Effect of hypoxemia and ethacrynic acid on ABR and distortion product emission thresholds.

Various studies have shown that induction of hypoxemia in animals such that arterial blood oxygen tensions reach 20-30 mm Hg is accompanied by reversible threshold elevations of the auditory nerve-brain-stem evoked response (ABR). In this state, the endocochlear potential (EP) is depressed, causing a smaller potential difference across the hair cells and/or reduced activity of the cochlear amplifier of the outer hair cells. In order to test these possibilities, ABR threshold (an expression of the overall sensitivity of the cochlea) and changes in threshold of the cubic (2f1-f2) distortion product emissions (DPE) (an expression of activity of the cochlear amplifier) were measured in the same cats while the EP was depressed by hypoxemia or by ethacrynic acid. During the episodes of hypoxemia, DPE thresholds were elevated by 10 dB while ABR thresholds were elevated by 22.8 dB. Therefore, it seems that a normal EP is necessary both for normal cochlear transduction (inner hair cells) and for normal cochlear amplification (outer hair cells). The human fetus in utero is relatively hypoxic and there is evidence that its auditory threshold is also similarly elevated. Therefore the threshold elevation in the fetus in utero, estimated to be about 20 dB, is a consequence of both reduced transduction current through the inner hair cells (about 10 dB) and an additional 10 dB reduction in the activity of the cochlear amplifier of the outer hair cells.

Animals↗
PubMed1995

Visual evoked potential abnormalities in jaundiced Gunn rats treated with sulfadimethoxine.

The manifestations of bilirubin encephalopathy include disturbances in the visual pathway (visual gaze paralysis and distorted visual perception). In the young jaundiced Gunn rat (jj) model of hyperbilirubinemia, significant differences in visual evoked potential (VEP) patterns have been recorded during development. In the present study, the effects of sulfadimethoxine (SDM) on VEP and electroretinogram (ERG) were examined in 3-wk-old jj rats. This drug displaces bilirubin from its albumin binding sites in the circulation, shifting it into tissues including the brain. Marked latency prolongations (11-20%) and reduced amplitudes (20-64%) were observed in the different wave components of the VEP. These changes were evident as early as 2 h after injection of the drug and persisted thereafter for another 4 h. On the other hand, ERG changes (significant prolongation of wave b) became apparent in these animals only 6 h after SDM injection. These results suggest that, although some changes in the retina may occur after a massive entry of bilirubin into the nervous system, the primary damage in the visual pathway after bilirubin exposure is probably beyond the retina.

Animals↗